Independent modulation of galactose-specific receptor expression in rat liver cells

The expression of galactose-specific receptors on liver cells from rats at the end of pregnancy and from estrogen-treated animals was studied. The number and distribution of binding sites were estimated on hepatocytes and Kupffer and endothelial cells in vitro as well as in situ by means of protein-gold complexes. Hepatocytes and endothelial cells from pregnant rats showed an increased binding activity of at least three times for hepatocytes and one and a half times for endothelial cells with respect to normal rat livers. The increase in the hepatocyte receptor expression was paralleled by an increase in the level of its specific messenger RNA (mRNA). On Kupffer cells, a decreased number of binding sites, at least three times less than control values, was measured. The correlation between the altered hormonal level during pregnancy and the expression of galactose binding sites was examined in hepatocytes and Kupffer cells isolated from virgin rats treated with the synthetic estrogen diethylstilbesterol. In estrogen-treated rats both the binding sites and the specific mRNA of hepatocytes increased as compared with vehicle-treated or untreated animals. In contrast, in Kupffer cells both the estrogen treatment as well as vehicle-only injection led to a significant reduction in the expression of binding sites as compared with virgin untreated animals. To establish whether the decrease of galactose binding sites in Kupffer cells was related to the activation of macrophages or to the removal of plasma membrane caused by enhanced nonspecific phagocytosis, in situ binding experiments were performed after lipopolysaccharide (LPS)-stimulation or latex-bead phagocytosis. Nonspecific phagocytosis does not affect the binding activity, which instead appears strongly reduced after LPS injection. These findings suggest an independent response of galactose-specific receptor expression systems in the different types of liver cells to modulating agents.